Cronin R E, Thompson J R
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas.
Miner Electrolyte Metab. 1991;17(2):100-5.
Potassium depletion can potentiate several experimental models of acute renal failure. It causes renal vasoconstriction, probably under the influence of vasoconstrictor prostaglandins and angiotensin II, and causes a reduction in vasodilatory prostaglandins. Aminoglycoside nephrotoxicity in experimental animals and in man causes a reduction in serum potassium and in animals it enhances the functional and histological damage produced by aminoglycosides. Chronic potassium loading protects against mercuric chloride, uranyl nitrate, and gentamicin models of acute renal failure. In the gentamicin model, protection is associated with a stimulation of renal cortical Na-K-ATPase activity and a reduction in the level of gentamicin accumulated in cortical tissue. In the clinical setting, potassium deficiency should be avoided in patients at risk for acute renal failure. However, potassium loading should also be avoided, since a falling glomerular filtration rate in the presence of a potassium load could result in potentially serious hyperkalemia.
钾缺乏可增强多种急性肾衰竭的实验模型。它会导致肾血管收缩，可能是在血管收缩性前列腺素和血管紧张素II的影响下，并导致血管舒张性前列腺素减少。实验动物和人类中的氨基糖苷类肾毒性会导致血清钾降低，在动物中，它会增强氨基糖苷类药物产生的功能和组织学损伤。慢性钾负荷可预防急性肾衰竭的氯化汞、硝酸铀酰和庆大霉素模型。在庆大霉素模型中，保护作用与肾皮质钠钾ATP酶活性的刺激以及皮质组织中积累的庆大霉素水平的降低有关。在临床环境中，急性肾衰竭风险患者应避免钾缺乏。然而，也应避免钾负荷，因为在存在钾负荷的情况下肾小球滤过率下降可能导致潜在的严重高钾血症。
